Thyroid disorders, thyroid autoimmunity, and anxiety-a systematic review and meta-analysis of population-based studies.

Comorbid insomnia and obstructive sleep apnea (COMISA) represent the coexistence of two of the most prevalent sleep disorders, yet accumulating evidence suggests that this overlap reflects more than incidental comorbidity. Insomnia symptoms are reported in approximately 40–60% of patients with obstructive sleep apnea (OSA), and 30–40% of individuals presenting with chronic insomnia meet diagnostic criteria for OSA when systematically evaluated [, ]. Despite this substantial overlap, insomnia and OSA are often assessed and managed within separate diagnostic pathways, contributing to underrecognition of their interaction and incomplete therapeutic response. Contemporary literature increasingly supports the view that COMISA constitutes a distinct and clinically consequential phenotype characterized by biological interaction rather than simple coexistence []. The burden associated with COMISA exceeds that of either disorder alone. Compared with isolated insomnia or OSA, patients with COMISA demonstrate greater sleep fragmentation, reduced sleep efficiency, lighter sleep-stage predominance, and higher rates of psychiatric comorbidity [, ]. In neurological and psychiatric populations, the combined phenotype has been associated with poorer global functional status and greater overall impairment, suggesting that COMISA may act as a disease modifier rather than merely a comorbid diagnosis []. Longitudinal data further demonstrates steeper decline in work ability among individuals with COMISA compared with those with either disorder independently, highlighting broader societal implications []. Longitudinal population-based analyses further demonstrate steeper declines in work ability among individuals with COMISA compared with those with either disorder independently, reinforcing broader socioeconomic implications (6). COMISA is strongly associated with reduced work ability, with individuals at high risk for COMISA having 5.7 times higher odds of poor work ability compared to those without sleep disorders []. The impact was most pronounced in workers below 60 years, white-collar workers, and daytime workers. Phenotypic heterogeneity further complicates clinical management. COMISA presentations vary according to objective sleep duration, psychiatric comorbidity, autonomic profile, and OSA endotype characteristics, and these differences influence treatment adherence and response. Baseline insomnia severity predicts poorer positive airway pressure adherence, while positive airway pressure (PAP) adherence influences insomnia trajectory, reflecting bidirectional interaction between respiratory stabilization and sleep continuity. Collectively, available evidence supports conceptualizing COMISA as a phenotype defined by mechanistic convergence between ventilatory instability and chronic hyperarousal, expressed through heterogeneous clinical presentations and associated with amplified cardiometabolic and functional burden. An integrated framework is therefore required to understand its epidemiology, mechanistic underpinnings, and clinical implications.